Article ID Journal Published Year Pages File Type
2190881 Journal of Molecular and Cellular Cardiology 2011 12 Pages PDF
Abstract

Mast cells are multifunctional cells containing various mediators, such as cytokines, tryptase, and histamine, and they have been identified in infarct myocardium. Here, we elucidated the roles of mast cells in a myocardial infarction (MI) rat model. We studied the physiological and functional roles of mast cell granules (MCGs), isolated from rat peritoneal fluid, on endothelial cells, neonatal cardiomyocytes, and infarct heart (1-hour occlusion of left coronary artery followed by reperfusion). The number of mast cells had two peak time points of appearance in the infarct region at 1 day and 21 days after MI induction in rats (p < 0.05 in each compared with sham-operated heart). Simultaneous injection of an optimal dose of MCGs modulated the microenvironment and resulted in the increased infiltration of macrophages and decreased apoptosis of cardiomyocytes without change in the mast cell number in infarct myocardium. Moreover, MCG injection attenuated the progression of MI through angiogenesis and preserved left ventricular function after MI. MCG-treated cardiomyocytes were more resistant to hypoxic injury through phosphorylation of Akt, and MCG-treated endothelial cells showed enhanced migration and tube formation. We have shown that MCGs have novel cardioprotective roles in MI via the prolonged survival of cardiomyocytes and the induction of angiogenesis.

Graphical AbstractFigure optionsDownload full-size imageDownload high-quality image (111 K)Download as PowerPoint slideResearch Highlights► The number of mast cells had two peak time point of appearance into infarct region. ► MCGs increased the infiltration of macrophage and decreased the apoptosis of CMs. ► MCGs attenuated the progression of myocardial infarction (MI) through angiogenesis.. ► MCGs-treated CMs were more resistant to hypoxic injury. ► MCGs-treated endothelial cells showed enhanced migration and tube formation.

Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Cell Biology
Authors
, , , , , , , , , , , ,